Polykaryocyte formation induced by VSV in mouse L cells.

Area of Science:

• Virology
• Cell Biology
• Immunology

Background:

• Vesicular stomatitis virus (VSV) infection is known to induce cell fusion in certain cell types.
• Understanding the mechanisms of VSV-induced cell fusion is crucial for comprehending viral pathogenesis and host-pathogen interactions.

Purpose of the Study:

• To investigate the kinetics and cell-type specificity of polykaryocyte formation induced by VSV infection.
• To elucidate the role of viral replication and host cell factors in VSV-mediated cell fusion.

Main Methods:

• Infection of various mouse and other cell lines (L, C-243-3, BHK, RK-13, PS, Vero) with VSV.
• Addition of anti-VSV immune serum and cycloheximide at different time points post-infection (p.i.) to assess their impact on cell fusion.
• Co-cultivation of infected and uninfected cells to evaluate cell-type specific fusion responses.

Main Results:

• VSV infection of mouse L cells induced polykaryocyte formation between 4-12 hours p.i.
• Suppression of viral replication with anti-VSV serum or cycloheximide (added within 1h p.i.) inhibited cell fusion.
• Cell fusion efficiency varied significantly among cell types, with L and C-243-3 cells showing high polykaryocytosis, while PS and Vero cells showed none unless co-cultivated with infected L cells.

Conclusions:

• VSV-induced cell fusion is dependent on viral replication and sensitive to inhibitors early in infection.
• The development of cell fusion is cell-type specific, suggesting distinct cellular permissiveness or regulatory mechanisms.
• Co-cultivation experiments indicate the potential involvement of cell-cell interactions or secreted factors in mediating fusion in non-permissive cells.